The past decade has witnessed hundreds of reports declaring or not being able to replicable genetic association with systemic lupus erythematosus (SLE) susceptibility. BANK1 is a gene that encodes a B-cell-specific scaffold protein and its activation can affect B-cell-receptor-induced calcium mobilization from intracellular calcium stores. TNFAIP3 encodes the ubiquitin-modifying enzyme, also known as A20, which is a cytoplasmic zinc finger protein that inhibits nuclear factor kappa-B (NFKB) activity and tumour necrosis factor (TNF)-mediated programmed cell death. The association of BANK1 and TNFAIP3 polymorphism with SLE has been reported in several studies. The aim of this study was to assess whether combined evidence shows the association between BANK1 and TNFAIP3 polymorphism and SLE. We report the results of a meta-analysis of genome-wide association scans and replication in independent sets for BANK1 and TNFAIP3 polymorphism and SLE that includes 12,416 subjects with SLE and 19,113 control subjects. Meta-odds ratios (ORs) and 95% confidence intervals (CIs) based on random effects models. Both of BANK1 and TNFAIP3 harbour several controversial single nucleotide polymorphisms (SNPs). We selected and identified three SNPs of BANK1 associated with SLE (rs17266594, P = 1.949e-10; OR = 1.380; 95% CI: 1.250-1.525; rs10516487, P = 2.642e-13; OR = 1.317; 95% CI: 1.223-1.417; rs3733197, P = 3.452e-06; OR = 1.193; 95% CI: 1.107-1.286); one SNP of TNFAIP3 associated with SLE (rs2230926, P = 1.502e-12; OR = 1.826; 95% CI: 1.545-2.157). This meta-analysis demonstrates a significant association between BANK1 and TNFAIP3 gene polymorphism and SLE in multiple ethnic populations. These findings reinforce the value of large sample series for discovery and follow-up of genetic variants contributing to the aetiology of SLE.
Many studies have examined the interaction between CYP1A1 MspI gene polymorphism and smoking for the risk of lung cancer risk in Chinese, but their results have been inconsistent. Therefore, a meta-analysis was performed to ascertain this issue. PubMed, Springer Link, Ovid and other Chinese databases were searched to include all the relevant studies. Smoking status was categorised as 'smokers' and 'non-smokers.' The pooled odds ratios (ORs) with 95% confidence intervals (CIs) were calculated using fixed or random effect model. Subgroup analyses according to ethnicity, source of control and geographical location were also conducted. This meta-analysis identified 13 studies containing 2248 lung cases and 3079 controls. Overall, a significant association between lung cancer and the variants of CYP1A1 MspI was found among smokers (type B and type C combined vs. type A: OR = 1.89, 95% CI = 1.15-3.11, P = 0.000 for heterogeneity), whereas not found among non-smokers. Similar to the overall results, stratified analyses showed that the increased risk of lung cancer was observed in population-based studies and north China among smokers (OR = 1.65, 95%CI = 1.03-2.66; OR = 2.00, 95% CI = 1.14-3.53). Our meta-analysis showed that there was an interaction between the CYP1A1 MspI and smoking on the risk of lung cancer in the Chinese population.
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